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Disruption of Endocrine Rhythms in Sleeping Sickness With Preserved Relationship Between Hormonal Pulsatility and the REM-NREM Sleep Cycles

Laboratoire de Physiologie et de Psychologie Environnementales, Strasbourg, France

A. Buguet

Centre de Recherches du Service de Santé des Armées Emile Pradé, La Tronche, France

K. Spiegel

Laboratoire de Physiologie et de Psychologie Environnementales, Strasbourg, France

A. Stanghellini

Service des Grandes Endémies, Ministère de la Santé, Brazzaville, Congo

G. Muanga

Département de Neurologie, Centre Hospitalier Universitaire, Brazzaville, Congo

P. Bogui

Laboratoire de Physiologie, Faculté de Médecine d'Abidjan, Côte d'Ivoire

M. Dumas

Institut de Neurologie Tropicale, Faculté de Médecine de Limoges, France

In human African trypanosomiasis (sleeping sickness), sleep and wake episodes are sporadically distributed throughout the day and the night. To determine whether these sleep disturbances affect the 24-h hormone profiles and the normal relationships between hormone pulsatility and sleep stages, poly-graphic sleep recordings and concomitant hormone profiles were obtained in 6 African patients with sleeping sickness and in 5 healthy African subjects selected from Abidjan on the Ivory Coast. Polysomnographic recordings were continuous, and blood was taken every 10 min throughout the 24-h period. Plasma was analyzed for cortisol, prolactin, and plasma renin activity (PRA). The 24-h rhythm of cortisol, considered to be an endogenous circadian rhythm, was attenuated in all of the patients except one. However, as in normal subjects, slow wave sleep (SWS) remained associated with the declining phases of the cortisol secretory episodes. Prolactin and PRA profiles, which are strongly influenced by the sleep-wake cycle, did not manifest the nocturnal increase normally associated with the sleep period; instead, they reflected a sporadic distribution of the sleep and wake episodes throughout the 24-h period. In patients with sleeping sickness as in normal subjects, rapid eye movement (REM) sleep began during the descending phases of prolactin pulses. In both groups, PRA reflected the sleep stage distribution with non REM (NREM) sleep occurring during the ascending phases and REM sleep during the descending phases of the PRA oscillations. However, in sleeping sickness patients, the marked sleep fragmentation often did not allow sufficient time for PRA to increase significantly, as is normally the case in subjects with regular NREM-REM sleep cycles. These results demonstrate that, together with the disruption of the sleep-wake cycle, there are profound differences in the temporal organization of the 24-h hormone profiles in humans with African trypanosomiasis. However, the relationship between hormonal pulses and specific sleep stages persists, indicating the existence of a robust link between hormonal release and the internal sleep structure.

Key Words: sleeping sickness • cortisol • prolactin • renin • circadian rhythm

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